Many minimally invasive surgical techniques and devices designed to reduce morbidity, expense, and the trauma associated with open-chest cardiac surgery have revolutionized cardiac surgery. Recent advances in endoscopic and thoracoscopic instruments and percutaneous access to a patient's thoracic cavity have made minimally invasive surgery possible. The advent of thoracoscopy in cardiac surgery has shown promise as a technique to enable surgeons to implant epicardial leads without sternotomy or thoracotomy. Thoracoscopy normally involves making small incisions between the ribs into the chest cavity and passing tubular ports Through the incisions. Illumination devices, cutting instruments, sutures, etc. may be inserted into the chest cavity via the ports. Approaches to accessing other sites of the left heart through the use of trocars and the racoscopes and various tools are described in U.S. Pat. Nos. 5,871,532 and 5,464,447, for example.
Other methods and apparatus that are introduced through percutaneously placed ports or directly through small trans-thoracic incisions for accessing the pericardial space employ suction devices to grip the pericardium or epicardium as disclosed, for example, in U.S. Pat. Nos. 4,991,578, 5,336,252, 5,827,216, 5,868,770, 5,972,013, 6,080,175, and 6,231,518. The suction devices are typically configured like a catheter or tube having a single suction lumen and typically having a further instrument delivery lumen. The suction lumen terminates in a single suction lumen end opening through the device distal end in the '578, '252, '175, '770, and '013 patents and through the device sidewall in the '216 and '518 patents. Certain of these patents recite that the applied suction draws a “bleb,” i.e., a locally expanded region of the pericardium, into the suction lumen or a suction chamber at the device distal end. A needle can then be advanced into the bleb and used to draw off fluids or deliver drugs into the pericardial space, or the like. In addition, it is suggested in these patents that treatment devices including catheters, guidewires, and electrodes, e.g., defibrillation electrodes, can be advanced into the pericardial space through a device introduction lumen for a variety of reasons. Although theoretically plausible, the ability to reliably maintain a vacuum seal against the pericardium when such treatment devices are advanced can be problematic.
One particular proposed use of such devices and procedures is to implant cardiac pacing and/or cardioversion/defibrillation leads, particularly to attach the electrodes of such leads to or within the heart wall.
In the field of cardiac stimulation, cardiac pacing leads having bipolar and unipolar pace/sense electrodes have long been used in conjunction with implantable pulse generators (IPGs) to conduct pacing pulses or cardioversion/defibrillation shocks generated by the IPG to a site of the heart and cardiac signals from the site to the IPG. Cardioversion/defibrillation leads and pacing leads are typically provided with a passive fixation or an active fixation mechanism at the lead body distal end that is passively or actively engaged with cardiac tissue to anchor a distal tip electrode at a desired site in or on the heart. Passive fixation generally involves an atraumatic fixation lodging the distal electrode against the endocardium or within a coronary blood vessel. Positive or active fixation generally involves a more traumatic penetration of a fixation mechanism into the myocardium from an endocardial or epicardial surface, and the active fixation mechanism commonly comprises a distal electrode.
Endocardial pacing and cardioversion/defibrillation leads having either active fixation or passive fixation mechanisms are implanted by a transvenous route into a heart chamber to locate the distal electrode(s) at a selected site in the heart chamber where an active or passive fixation mechanism is deployed to maintain the electrode affixed at the site. Epicardial leads are implanted by exposure of the epicardium of the heart typically through a limited subxiphoid approach or a more extensive surgical exposure made to perform other corrective procedures. The distal end of the epicardial lead formed with one or two electrodes and an active fixation mechanism supported by an electrode head is affixed to the epicardium. Typically, the active fixation mechanism comprises the single electrode or one of the bipolar electrodes, but can be separate and electrically isolated from the electrodes.
Epicardial pacing and cardioversion/defibrillation leads were the first to be implanted widely, because endocardial leads lacked effective active or passive fixation mechanisms and relied upon relatively stiff lead bodies that cause perforations and dislodgement of the distal electrode(s) or fracture of the lead conductor. Initially, access to the epicardium was made by a thoracotomy or median sternotomy and excision through or removal of the pericardial sac. Typically, pace/sense electrodes penetrated the myocardium and were sutured against the epicardium to maintain fixation. The large surface area patch electrodes of cardioversion/defibrillation electrodes were sutured to the epicardium.
Improvements were made in epicardial pace/sense leads to reduce the surgical trauma involved in accessing the epicardium and to avoid the need to suture the electrode to the epicardium through the use of active fixation mechanisms. Such active fixation mechanisms of epicardial pacing leads typically comprise a tissue penetrating, self-affixing mechanism extending away from a support or base or plate of the electrode head. The fixation mechanism is forced into the myocardium typically employing an introduction tool engaging the electrode head until it is fully seated within the endocardium and the plate bears against the epicardium. The plate is typically formed with a tissue ingrowth encouraging fabric or lattice, whereby tissue ingrowth about the plate assists in chronic anchoring to the heart. Such active fixation mechanisms typically comprise either or both of a helix or hook having a sharpened tip that is coupled with a lead conductor within the electrode head.
An active fixation, unipolar, epicardial lead having a barbed hook is disclosed in commonly assigned U.S. Pat. No. 4,313,448 and embodied in the MEDTRONIC® Model 6951 lead. The active fixation mechanism comprises forward facing barbed electrode having the tip at a predetermined angle with relation to the shank of the electrode and with respect to a flexible base pad or plate of the electrode head. The plate has a substantially centered hole and a plurality of outer holes for fibrous ingrowth, and the shank of the electrode extends out through the substantially centered hole. The barbed electrode is pushed into the myocardial tissue to the point where the base pad engages against the epicardium thereby indicating full implantation within the myocardium. During implantation, a stiffening stylet is employed to stiffen the lead body and a forceps is employed to grasp the electrode head to push the barb into the myocardium.
The MEDTRONIC® Model 6917 epicardial pacing lead and subsequently introduced epicardial pacing lead models support the helix to extend at 90° to the plate as disclosed in commonly assigned U.S. Pat. Nos. 3,737,579 and 4,010,758. Other variations of such epicardial screw-in leads include multiple co-axial and intertwined helixes or a helix axially surrounding a pin extending coaxially with the helix axis from the electrode head. During implantation, the lead body and electrode head are mounted to an elongated implantation tool, and the sharpened tip of the helix is advanced through the incision to perforate the epicardium. The tool and lead are rotated to screw the helix into the myocardium until the plate abuts the epicardium, and the electrode head is detached from the tool. Alternatively, the sides of the electrode head are grasped by tongs and that are rotated to screw the helix into the myocardium until the plate abuts the epicardium, and the electrode head is detached from the tongs as disclosed in commonly assigned U.S. Pat. No. 6,010,526.
A further epicardial screw-in lead is disclosed in commonly assigned U.S. Pat. No. 4,357,946 wherein the helix is mounted to a gear mechanism within the electrode head. The helix can itself be rotated to screw into the myocardium without rotating or moving the electrode head by a rotation of a removable stylet extending through the length of the lead body and engaging the gear mechanism. Both unipolar and bipolar embodiments are disclosed.
The implantation of such epicardial leads is usually through general thoracic surgery; either via a median sternotomy or intercostal approach or via a more limited subxiphoid approach. These procedures involve major surgery that may be painful and dangerous for the patient and can be costly. The subxiphoid approach, moreover, only permits limited access to the anterolateral surface of the left ventricle and does not provide any access at other locations of the left ventricle or the left atrium.
By contrast, the percutaneous implantation of endocardial leads became much less traumatic, faster, and less costly, and the deficiencies of early endocardial pacing leads were overcome. Over the years, endocardial pacing leads were improved by incorporation of effective and easy to use active and passive fixation mechanisms to overcome the problems of dislodgement. Moreover, lead bodies were made stronger, more flexible, smaller in diameter, and more reliable. Fixation of pace/sense electrodes in the right atrium, right ventricle and within the coronary sinus and great vein descending from the coronary sinus became possible. Endocardial cardioversion/defibrillation leads were also developed incorporating these improved features of pacing leads and elongated cardioversion/defibrillation electrodes for implantation in the same locations.
Because of these improvements, endocardial pacing and cardioversion/defibrillation leads largely supplanted epicardial pacing and cardioversion/defibrillation leads in clinical practice. Epicardial pacing leads remained medically indicated for some patients, particularly children, or patients undergoing oven heart surgery for other reasons. Although the various indications for epicardial lead fixation in pediatric patients are numerous, some common factors include small stature, congenital heart defects with residual or potential right to left shunting or single ventricle hearts, or lack of venous access to the chamber requiring pacing.
The left ventricle has a greater wall thickness (10–20 mm as compared to 1–5 mm) than the right ventricle because the left ventricle of the heart must pump oxygenated blood throughout the body while the right ventricle only pumps venous blood through the lungs to be oxygenated. Because the left heart is relatively more important for hemodynamic output, not surprisingly, various pathologies may be better treated through pacing of the left heart. For example, in patients with dilated cardiomyopathy and congestive heart failure, electrical stimulation of both the right and left heart chambers has been shown to be of major importance to improve the patient's well being and manage heart failure. See, for example, Cazeau et al., “Four Chamber Pacing in Dilated Cardiomyopathy,” PACE, November 1994, pgs. 1974–79. See also the pacing systems providing synchronized right and left heart chamber pacing of heart failure patients disclosed in U.S. Pat. Nos. 5,716,392, 5,902,324, and 6,219,579. Recently, several right and left heart pacemakers and implantable cardioverter-defibrillators incorporating right and left heart pacing functions have been approved for clinical implantation in patients suffering from congestive heart failure.
Endocardial pacing electrodes cannot be implanted directly within the left heart chambers due to risk of thrombus formation about the lead body and electrode surfaces. Blood flows through the right heart chambers (atrium and ventricle), through the lungs, through the left heart chambers (atrium and ventricle) and then through the rest of the body, including the brain, before returning again to the right atrium. Implanted objects often cause minor blood clots and thrombus to form in the blood. These may, on occasion, dislodge and be released into the bloodstream. Any blood clots or thrombi, however minor, that form in the left atrium and ventricle could have serious consequences if they were to break free and be swept into the brain and cause a stroke. In contrast, clots or thrombi released from an object implanted in the right side of the heart would simply travel to the lungs, where they would lodge, usually without serious risk.
Consequently, endocardial leads are directed through the coronary sinus to locate pace/sense or cardioversion/defibrillation electrodes in the coronary sinus or great vein in order to pace and sense and/or cardiovert/defibrillate the left heart. The possible sites for lodging the pacing and/or cardioversion/defibrillation electrodes relative to the left atrium or left ventricle are necessarily limited by the coronary sinus and great vein. At times it is difficult to advance the pacing and/or cardioversion/defibrillation electrodes into or to a desired site of the coronary sinus or great vein. And, the lead bodies tend to fibrose into the coronary sinus or great vein over time and become difficult or impossible to remove if it becomes desirable to do so.
Therefore, interest in implanting epicardial pacing and cardioversion/defibrillation electrodes at a variety of left heart sites to provide the most efficacious left and right heart pacing for the patient suffering from congestive heart failure has increased in recent years.
Despite these improvements a need exists for a simple way to attach a pace/sense electrode of a pacing lead to the epicardium or to perform various other procedures through a small diameter transthoracic port or incision.